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Latent transforming growth factor binding protein 4 (LTBP‐4) is downregulated in human mammary adenocarcinomas in vitro and in vivo
Author(s) -
MAUEL SUSANNE,
KRUSE BIANCA,
ETSCHMANN BENJAMIN,
VON DER SCHULENBURG ANNABELLE GRÄFIN,
SCHAERIG MONIKA,
STÖVESAND KIRSTEN,
WILCKEN BJÖRN,
STERNERKOCK ANJA
Publication year - 2007
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2007.apm_453.x
Subject(s) - transforming growth factor , downregulation and upregulation , mammary gland , in vivo , transforming growth factor beta , carcinogenesis , biology , cancer research , in vitro , cell culture , cell growth , mammary tumor , extracellular , transcription factor , endocrinology , medicine , microbiology and biotechnology , cancer , biochemistry , gene , genetics , breast cancer
Transforming growth factor beta (TGF‐ß) is able to inhibit proliferation of epithelial cells and is involved in the carcinogenesis of human mammary tumours. Three latent transforming growth factor‐ß binding proteins (LTBP‐1, ‐3 and ‐4) are involved in TGF‐ß function. The aim of the study was to analyze the expression profiles of TGF‐ß 1 and 2 and LTBP‐4 in human mammary carcinoma cell lines as well as in human mammary tumours. Expression analysis was performed at the transcription and protein level under in vivo and in vitro conditions. LTBP‐4 expression was quantitatively analysed in human carcinomas of the mammary gland and in healthy mammary tissues of the same patients. Downregulation of LTBP‐4 in all investigated human mammary tumours compared to normal tissues could be demonstrated. Results also revealed that protein levels of TGF‐ß 1 are downregulated and of TGF‐ß 2 are upregulated in human mammary carcinoma cell lines compared to primary (normal) human mammary epithelial cells. LTBP‐4 reduction in neoplasms leads to a possible decrease of TGF‐ß 1 extracellular deposition with reduced TGF‐ß 1 bioavailability. TGF‐ß 2 was upregulated, which indicates a possible compensatory mechanism. This study demonstrated a possible functional role of LTBP‐4 for TGF‐ß bioavailability with respect to carcinogenesis of human mammary tumours in vivo and in vitro .

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